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Direct-MS wrote: For example smoking is a risk factor for MS and thus it is wise not to smoke. Similarily CCSVI is a risk factor for MS and thus if you have CCSVI and MS it would be wise to get it repaired.

I realize this is not what many people on this forum want to hear but it is critical to be as objective as possible and accept what the science says. It is important to get CCSVI relieved but it is perhaps more important to address the autoimmune nature of MS. Trying to rationalize the Buffalo data to hold on to the concept that CCSVI is the primary cause of MS is not productive.

First of all there is no evidence about smoking triggering MS whatsoever. There are SOME indications that it may contribute to progression simply because IT BLOCKS VESSELS all over the body and the cns but there are studies that failed to prove the relation. Maybe we shouldn't use examples of any previous point outs and have in mind that ccsvi is brand new, exploring pathways that have never been touched by the science before.

They ARE addressing the autoimmune nature of MS for the last 80 years and where did it lead them? To destroy our immune system to prevent it from causing damage. Did it help? No.
In other words, if CCSVI wont do the trick they should explore other similar pathologies in order to cure MS someday.
Dr Coles recently stated: "MS cure will not be found for at least 30 to 40 years and this goes with almost all autoimmune diseases". This is a from a major contrimputor to the "autoimmune nature" research.

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bluesky63 wrote:When I went to sign up for the Buffalo study in the first place, I saw that they were *excuding* anyone who had any sort of venous abnormality that they already knew about. I wondered if that would skew their results, because it would potentially exclude people who would then end up showing CCSVI. For instance, some of the members here have mentioned venous angiomas, and at least two of those people have subsequently been found to have stenosis (not at Buffalo).

Wouldn't it have been more reasonable for the purpose of this study to just take people with MS no matter when their venous status?

I find this, together with the CIS inclusion, the most likely cause of the "low" correlation CCSVI-MS. Is there any candidate rejected for venous problems before the trial?

(i) There is no causality effect between vein narrowing and MS. Narrowing occurs as a symptom of the disease (like itching, blindness and else) for half of the patients.

(ii) OR, CCSVI is a factor leading to MS. The fact that only 50% have it coincides with the statistic that 50% go into Phase 2 (Secondary progressive), while the rest are stabilizing as the veins open after a while. So the one who still have narrowing (say after 10-15 years from disease discovery) are on a bad course.

(i) There is no causality effect between vein narrowing and MS. Narrowing occurs as a symptom of the disease (like itching, blindness and else) for half of the patients.

(ii) OR, CCSVI is a factor leading to MS. The fact that only 50% have it coincides with the statistic that 50% go into Phase 2 (Secondary progressive), while the rest are stabilizing as the veins open after a while. So the one who still have narrowing (say after 10-15 years from disease discovery) are on a bad course.

Any thoughts?

I still don't see how MS could cause CCSVI considering that CCSVI manifests itself in so many ways. I mean, if CCSVI was simply the cell walls of the vein were larger than usual and hurt blood flow then ok, maybe, but we have CCSVI cases where people have veins pinched by bones, cases where people have jugular veins that are too short, cases where the veins are too wide, cases with missing veins or misfunctioning valves, etc. It doesn't make sense to me that MS would cause a variety of competely different scenarios that lead to the end problem of reflux of blood into the brain.

I find the 55%/62% numbers a little discouraging with the 80% being a little more comforting. We'll just have to see how this plays out with additional studies.

Motiak wrote:I find the 55%/62% numbers a little discouraging with the 80% being a little more comforting. We'll just have to see how this plays out with additional studies.

In comparison to the Zamboni study it is not a so much difference. Zamboni had another exclusion criteria. He did not have any CIS and unclear doppler results. If you consider:

The researchers also found fewer cases of CCSVI in patients who had experienced a single MS attack, called clinically isolated syndrome, compared to those with more advanced symptoms of the disease —38 per cent versus about 80 per cent.http://www.healthzone.ca/health/newsfea ... f-ms-study

you have in the RRMS group 80%. That are the numbers you have to compare to the Zamboni study.

Prof8-I think that you actually confirmed my statement... anemia is not normal iron metabolism! It is amazing how many people are showing up with some form of anemia or some form of high ferritin or some form of high transferrin saturation etc. Maybe there is a relationship between the different forms of abnormal iron metabolism and stenosis etc. Perhaps the low ferritin is an indication of higher inclination to the CCSVI... there is no reason to not run a simple blood test when they are doing all of this investigation into iron deposits in the brain. Iron is also found in the brains of people with Parkinson's, and people with Alzheimer's... which tells me that all of these neurodegenerative diseases must have a mechanism whereby iron ends up in the wrong places. For instance, you have high transferrin saturation besides the anemia? If so, the transferrin would be putting iron into the wrong places instead of the liver... we need to investigate just how many people with MS seem to have skewered iron profiles. I also think we need to look at the ratios of these iron results. It would be so easy to collect a good database when you are bringing all of these people together at one time. I do not buy your dismissal of the blood test theory at all that would be still useful to look at a broad population of people with MS and their iron status... sorry but it is just a blood test! I was also anemic when I was in my teens and 20s... now I believe that I am iron loading and all the wrong places. When you look at the studies concerning T cells and iron, you get another avenue whereby the autoimmunity factor could kick in.

The idea of including all borderline patients in the negative column shows interesting assumptions made by the buffalo team.Like a courtroom where you are guilty until proven innocent. Its the long solid road its going to be slow.

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